Diagnosis and contraol of common diseases of hamsters, rabbits, and monkeys.
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Results for “MONKEY DISEASES”
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Pigmentary liver disease in howler monkeys.
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Agent of disease contracted from green monkeys.
An infectious agent obtained from patients who became ill after exposure to tissues of African green monkeys is viral in character. By electron microscopy, the agent appeared cylindrical, 90 to 100 nanometers in diameter, and 130 to 2600 nanometers in length. Cross-striations at 5-nanometer intervals and a core diameter of 45 nanometers were observed. The agent was completely resistant to the effects of the metabolic inhibitor 5-bromodeoxyuridine, which may mean that RNA is the genetic material. It was sensitive to ether and relatively sensitive to destruction by heat.
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Perivascular fibrosis of splenic follicular blood vessels in Macaca mulatta.
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Hydatid disease in a rhesus monkey.
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[Unknown viral disease transmitted from infected monkeys to man].
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Adult↗
Tuberculosis of the spine (Pott's disease) in a rhesus monkey (Macaca mulatta).
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The epizootics of Kyasanur Forest disease in wild monkeys during 1964 to 1973.
In the Kyasanur Forest disease area two species of wild monkeys, Presbytis entellus and Macaca radiata, succumb to the natural infection with Kyasanur Forest disease (KFD) virus (family Flaviviridae). Between October 1964 and September 1973, 1046 monkeys (860 P. entellus and 186 M. radiata) died. Of these, KFD virus was isolated from 118 P. entellus and 13 M. radiata. Maximum mortality of monkeys was reported during December through May coinciding with the season of activity of immature stages of Haemaphysalis ticks, incriminated vectors of KFD. The epizootic showed an initial spread of the disease to the areas contiguous with the original focus of infection. This was followed by the recognition of epizootics and epidemics in three new foci, removed from the original focus, by the end of 1973. It was also observed that, in certain localities in the original focus, KFD virus activity persisted over several years.
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Trypanosoma cruzi: experimental Chagas' disease in rhesus monkeys. II. Ultrastructural and cytochemical studies of peroxidase and acid phosphatase activities.
Ultrastructural and cytochemical studies of peroxidase and acid phosphatase were performed in skin, lymph node and heart muscle tissue of rhesus monkeys with experimental Chagas' disease. At the site of inoculation there was a proliferative reaction with the presence of immature macrophages revealed by peroxidase technique. At the lymph node a diffuse inflammatory exudate with mononuclear cells, fibroblasts and immature activated macrophages reproduces the human pattern of acute Chagas' disease inflammatory lesions. The heart muscle cells present different degrees of degenerative alterations and a striking increase in the number of lysosomal profiles that exhibit acid hydrolase reaction product. A strong inflammatory reaction was present due to lymphocytic infiltrate or due to eosinophil granulocytes associated to ruptured cells. The present study provides some experimental evidences that the monkey model could be used as a reliable model to characterize histopathological alterations of the human disease.
Acid Phosphatase↗
Genetic galactocerebrosidase deficiency (globoid cell leukodystrophy, Krabbe disease) in rhesus monkeys (Macaca mulatta).
Globoid cell leukodystrophy, or Krabbe disease, is a severe disorder of the peripheral and central nervous system myelin caused by deficient galactocerebrosidase (GALC) activity. This autosomal recessive disease affects humans and animals including dogs, mice, and rhesus monkeys. Cloning of the human and animal GALC genes opened opportunities for therapeutic trials using animal models. We describe the clinical, pathologic, and biochemical features of the affected rhesus monkey. Affected monkeys had very low GALC activity and a two base pair deletion in both copies of the GALC gene. Clinical signs of tremors, hypertonia, and incoordination led to humane euthanasia by 5 months of age. At necropsy, peripheral nerves were enlarged. Microscopically, the cerebral, cerebellar, and spinal cord white matter was infiltrated with periodic acid-Schiff-positive multinucleated globoid cells, and there was a striking lack of myelin. Peripheral nerve fibers were decreased in number and separated by Alcian blue- and safranin O-positive material. Myelin sheaths were greatly diminished. Lipid analysis of brains of 12-day-old and 158-day-old affected monkeys revealed a great excess of psychosine in white matter. The rhesus monkey model will be especially useful for exploring treatment options, including prenatal bone marrow transplantation and various approaches to gene therapy.
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EB virus in the owl monkey (Aotus trivirgatus).
Owl monkeys (Aotus trivirgatus) were inoculated with EB (Epstein-Barr) virus-containing material or virion-free control material. One out of three animals given the virus died after 14 weeks with a reticuloproliferative disease compatible with malignant lymphoma. A cell line was established from an abnormal lymph node of the diseased monkey and was found by electronmicroscopy to carry a herpesvirus identified as EB virus by two types of immunofluorescence test, by its biological behavior and by nucleic acid hybridization studies. None of the inoculated animals developed heterophile antibodies, and only the diseased animal had an antibody response to EB virus. The findings were discussed in relation to a possible oncogenic capacity of EB virus in vivo.
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Green monkey agent of disease.
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Nontuberculous mycobacterial disease in rhesus monkeys.
In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.
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Nontuberculous mycobacterial disease in rhesus monkeys.
In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.
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Rift Valley fever infection of rhesus monkeys: implications for rapid diagnosis of human disease.
Rhesus monkeys inoculated with Rift Valley fever (RVF) virus provide a model in which serial observations of serum viral antigen and antibodies can be made. In 9 non-fatal and 3 fatal infections, either antigen or IgM enzyme-linked immunosorbent assay (ELISA) antibodies were detected in every serum sample during the acute phase. Furthermore, viral nucleic acid could be detected by filter hybridization in most samples taken on days 1 to 3. Circulation of significant quantities of viral RNA provides an additional approach to the diagnosis and study of RVF.
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Experimental infection of monkeys with Herpesvirus suis (Aujeszky's-disease virus).
Monkeys were infected intranasally with Herpesvirus suis. After an incubation period of 7 to 13 days the animals became acutely ill and rapidly died. Clinical signs included salivation, incoordination, ataxia and epileptiform convulsions, but not pruritus. Histopathological changes were confined to the central nervous system, and consisted of destruction of neurones with the formation of intranuclear inclusion bodies, gliosis and perivascular cuffing. Virus was isolated from the brain and spinal cord in the later stages of the illness but neutralising antibodies were not detected in serum. The distribution of lesions indicated direct spread of virus from the inoculation site along cranial nerves to the brain.
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Endemic enteric disease in vervet monkeys.
Comprehensive bacteriological investigation indicates Shigellae as the probable aetiological bacteria in one endemic enteric disease situation. One species and four serotypes have been detected. In vitro antibiotic sensitivity spectra have been determined. Epidemiology, pathology and pathogenesis in relation to the experimental animal situation and experimental results are considered. A rationale for treatment and control is suggested.
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Simian virus 40-induced disease in rhesus monkeys with simian acquired immunodeficiency syndrome.
Simian virus 40 (SV40) disease was diagnosed in four rhesus monkeys that died with SIV-induced acquired immunodeficiency syndrome (AIDS). One juvenile monkey seroconverted for SV40 6 months after inoculation with SIV and developed severe bilateral tubulointerstitial nephritis. In contrast, progressive multifocal leukoencephalopathy (PML) occurred in two adult monkeys that were seropositive for SV40 before SIV inoculation, as well as a third adult that was naturally infected with SIV and seropositive for SV40 5 years before death. Large intranuclear inclusions containing abundant polyomavirus particles were limited to either renal tubular epithelial cells or oligodendrocytes. In situ DNA hybridization for SV40 large T antigen further demonstrated that SV40 nucleic acid was localized to either kidney or brain tissue. By immunohistochemical analysis, areas of central nervous system inflammation and demyelination were shown to contain CD68+ macrophages (gitter cells), aggregates of CD8+ T lymphocytes, and numerous gemistocytic astrocytes that labeled for glial fibrillary acidic protein. These observations indicate that rhesus monkeys with SIV-induced AIDS are predisposed to polyomaviral disease, in which SV40 nucleic acid is observed in renal tissue in primary infections and brain tissue after viral reactivation. Furthermore, this organ-specific replication suggests that tissue-tropic strains of SV40 may develop in immunodeficient monkeys.
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